At a constant minute ventilation, nitric oxide inhalation caused dose-independent decreases in Paco2 (p <.05), alveolar deadspace (p <.01), and arterial-to-end tidal CO2 partial pressure differences (p <.01). Each sheep breathed 0 ppm, 5 ppm, and 20 ppm nitric oxide in random order.Įstimates of alveolar deadspace volumes and arterial-to-end tidal CO2 partial pressure differences were used as indicators of CO2 elimination efficiency. To induce acute lung injury, hydrochloric acid was instilled into the tracheas of paralyzed sheep receiving controlled mechanical ventilation. Prospective, placebo-controlled, randomized, crossover model. To test the hypothesis that nitric oxide inhalation facilitates CO2 elimination by decreasing alveolar deadspace in an ovine model of acute lung injury.
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